Implantable cardiac devices are well known in the art. They may take the form of implantable defibrillators or cardioverters which treat accelerated rhythms of the heart such as fibrillation or implantable pacemakers which maintain the heart rate above a prescribed limit, such as, for example, to treat a bradycardia. Implantable cardiac devices are also known which incorporate both a pacemaker and a defibrillator (ICD).
A pacemaker may be considered as having two major components. One component is a pulse generator which generates the pacing stimulation pulses and includes the electronic circuitry and the power cell or battery. The other component is the lead, or leads, which electrically couple the pacemaker to the heart.
Pacemakers deliver pacing pulses to the heart to cause the stimulated heart chamber to contract when the patient's own intrinsic rhythm fails. To this end, pacemakers include sensing circuits that sense cardiac activity for the detection of intrinsic cardiac events such as intrinsic atrial events (P waves) and intrinsic ventricular events (R waves). By monitoring such P waves and/or R waves, the pacemaker circuits are able to determine the intrinsic rhythm of the heart and provide stimulation pacing pulses that force atrial and/or ventricular depolarizations at appropriate times in the cardiac cycle when required to help stabilize the electrical rhythm of the heart.
Pacemakers are described as single-chamber or dual-chamber systems. A single-chamber system stimulates and senses the same chamber of the heart (atrium or ventricle). A dual-chamber system stimulates and/or senses in both chambers of the heart (atrium and ventricle). Dual-chamber systems may typically be programmed to operate in either a dual-chamber mode or a single-chamber mode.
Implantable cardiac stimulation devices conventionally include an internal telemetry circuit permitting the devices to communicate with an external programmer. The external programmers also include a telemetry circuit with an external antenna or “wand” which is held over the implant site to allow the communication between the programmer and the implanted device. With the communication channel thus established, the programmer permits the attending medical personnel to set device operating modes and stimulation and sensing parameters within the device. The communication channel also permits the device to convey to the external programmer operating and sensed physiological data for display. The physiological data may include an intracardiac electrogram (IEGM). The IEGM may be prestored in the device and conveyed to the programmer responsive to a suitable external command from the programmer. The IEGMs are typically stored in response to high rate ventricular events or high rate atrial event triggers. The result is that physicians have more insight into the operation of the devices and have more information about the underlying rhythm that interacts with the device.
In addition to the IEGMs, physicians would like to be provided with a surface electrocardiogram (EKG). Their desire is based upon their day-to-day use of surface EKGs to make diagnosis of arrhythmias. Hence, with both IEGMs and surface EKGs, physicians will have more confidence that they will be able to discern exactly the underlying arrhythmic event that triggered the IEGM storage.
Unfortunately, implantable devices cannot provide surface EKGs. While some programmers of implantable cardiac stimulation systems do accommodate the display of surface EKGs, the surface EKGs available are taken at regular follow-up visits and thus after the arrhythmic event and IEGM storage have occurred. An after the fact surface EKG is not very helpful in support of a diagnosis of a prior arrhythmic episode.
Surface EKGs are particularly advantageous because they contain low frequency components suitable for measuring slowly changing EKG features. One such feature of preferred measure is the ST segment elevation. Measurement of ST segment elevation is very useful in diagnosing myocardial ischemia.
Myocardial ischemia results from insufficient blood flow to the heart muscle. Ischemia may occur chronically to varying degrees due to coronary artery disease (CAD) or acutely due to sudden increased demand, embolism or vasospasm. Ischemia can lead to angina and eventually to myocardial infarction resulting in permanent damage to the heart muscle. Both ischemia and infarction can trigger fatal arrhythmias.
In patients who have angina as a symptom of coronary artery disease, three to four episodes of silent ischemia (ischemia without angina) occur for every symptomatic episode. Objective evidence of ischemia, even when asymptomatic, is associated with negative clinical outcomes.
Ischemia can be detected by electrocardiographic changes. The classic electrocardiographic feature associated with myocardial ischemia (MI) is a change in the amplitude of the ST segment relative to the isoelectric baseline. Usually, a diagnostic 12-lead EKG is used. Detection through surface EKG is done only briefly and infrequently in the clinic or through the use of a holter monitor. Only those ischemic events which happen to occur, or which may be provoked by stress tests during monitoring are detected. The nature of electrocardiographic changes and the leads on which they appear are used to localize the region of ischemia.
A long-term record of ischemia burden obtained through continuous monitoring would be very useful as an adjunct to current methods of ischemia detection and diagnosis. Such a record may reveal infrequent or unprovokable ischemia, perhaps associated with nascent CAD, vasospasm or embolism. Such a record could reveal trends in the progression or regression of CAD. It could also be used to gauge the efficacy of, and/or patient compliance with, a course of medication.
Implantable medical devices (IMDs) such as pacemakers and ICDs offer an ideal platform for ischemia burden monitoring. IMDs can constantly monitor the electrophysiological conditions of patients and detect the onset and/or the burden of ischemia based on ST level change detected from IEGMs of implanted lead electrodes. Other applications may include alerting the patient of an ischemic episode which may not otherwise produce symptoms (silent MI), remotely notifying a physician or monitoring center upon MI detection, and releasing antithrombotic or thrombolytic medication upon MI detection.
A particular challenge exists for detection of MI via changes to the ST segment using pacemakers and ICDs. The challenge is that the ST segment is a slow-changing feature of the electrogram (voltage vs. time). Therefore, it would be required that the signal path of the IMD faithfully transmit low-frequency information if the ST segment is to be used for detection of MI. Pacemakers and defibrillators typically attenuate electrogram frequencies below 1 Hz. By comparison, the standard diagnostic ECG high pass filter cutoff frequency is 0.05 Hz. That is, frequency components are faithfully reproduced all the way down to 0.05 Hz.
Unfortunately, much of the useful information in the ST segment is carried by frequency components between 0.05 Hz and 1 Hz. Investigations have demonstrated that high pass filtering IEGMs with a 1 Hz cutoff significantly negatively impacts (compared to a 0.05 Hz cutoff frequency) the ability of MI detection algorithms to extract information from the ST segment useful to the task of MI detection. If the high-pass filter cutoff frequency were 0.25 Hz or lower, most of the ability of MI detection algorithms to effectively detect MI would be preserved.
One solution is to change the hardware of pacemakers or defibrillators to lower the high pass frequency cutoff. However, this solution by itself has potential negative effects. The high pass cutoff frequency of 1 Hz was chosen in pacemakers and ICDs for many good reasons. For example, the 1 Hz cutoff removes much of the respiration artifact from the IEGM. It also attenuates motion artifact. It also attenuates the unavoidable slow-changing voltage due to the slow recharge phase after a pacing pulse. This slow-recharge signal could be very large with high-polarizing leads.
If the IEGM channel high pass cutoff frequency is decreased, these formerly attenuated slow-changing signals will become larger relative to signals of interest, e.g. R-waves and T-waves. If they become large enough, there will be no way to prevent IEGM signals from being clipped prior to being digitized while still preserving sufficient resolution of the signals of interest. If clipping occurs, information is irretrievably lost and the usefulness of the IEGM channel is severely compromised or lost altogether unless the cutoff frequency change is performed by additional signal processing separate from the normal signal processing.
The measurement of slow-changing features of individual QRST complexes may be desirable for other purposes. For example, features of ST segment and T-wave morphology may be used to monitor blood glucose level or cardioactive drug action. Other slow-changing electrogram features include P-R segment elevation.
For measuring slow-changing EGM features, designing the pacemaker and ICD front end circuitry to lower the high-pass cutoff frequency would be ideal, as a high signal-to-noise ratio would be preserved throughout the signal path for all frequencies of interest. However such a design could have overall negative system impacts, foreseen and unforeseen. It would thus be desirable if the hardware front end could remain unchanged and IEGMs post-processed only as needed for ischemia detection or other purposes, thus eliminating the risks associated with such a hardware design.